Abstract This project will use a unique new data resource from the Health and Retirement Study (HRS) to elucidate multiple biological pathways through which life course social disadvantage ?gets under the skin? and influences subsequent morbidity and mortality. We will examine the association between social adversity and multiple composite measures related to basic processes of biological aging including clinical indicators of physiological status, immune system functioning, telomere attrition, mitochondrial depletion, DNA methylation, and gene expression in order to understand the mechanisms through which those of low socioeconomic status (SES) ?age? at a faster rate than persons with higher SES. The uniqueness of this project resides in the breadth and depth of the biological indicators which characterize some of the basic mechanisms of aging and have not been examined in a nationally representative population with ability to characterize SES differences. We expect that low socioeconomic status (SES), and related stressful life events, adverse psychological states, and poor health behaviors will be associated with worse physiological status, immunological functioning, methylation profile, adverse expression, more mitochondrial depletion, and shorter telomere length at a given chronological age. While low SES and accompanying life circumstances at any age are expected to be associated with late life biology, cumulative social disadvantage beginning in childhood and sustained throughout life is expected to have a multiplicative association in increasing adverse biological markers as we expect some biological processes to be more influenced by childhood circumstances and others by more current circumstances. We will examine the association of emotional, financial, and psychological costs of low SES in early and later life with biological outcomes and hypothesize that the effect of these different aspects of life will vary with timing and domain. We will also identify both genetic and social, psychological and environmental buffering factors that will reduce the association of low SES with adverse biological profiles. The outcome of this project will be the identification of a comprehensive-integrated set of measures that characterize the biological pathway from social adversity to poor health and ?explain? at a biological level why socially disadvantaged individuals are at greater risk of aging-related morbidity and mortality outcomes. Identifying multiple social and biological mechanisms that influence the pace of aging will enhance our understanding of the underlying causes of health disparities and the lifecycle processes by which they arise. This work will increase substantially our understanding of how predisposing factors (cellular and molecular changes, deterioration in the immune function, and physiological characteristics) and precipitating factors (socioeconomic status, psychosocial and environmental stressors, and health behaviors) together influence age- related health conditions (age-related morbidity and mortality).